In fasting dogs between 29 and 53 per cent (median 42 per cent) of newly produced bile was stored in the gall bladder, with the remainder being released directly into the duodenum. Pretreatment with methadone and atropine resulted in the complete closure of the sphincter of Oddi for three hours, and the complete retention of bile in the gall bladder. This effect could be abolished with nalorphine. The minimum dose of methadone to prevent bile from entering the intestines was 0.25 mg/kg, in combination with 0.1 mg/kg atropine. A meal of canned dog food resulted in the release of between 5 and 65 per cent of gall bladder bile (median 31 per cent) into the duodenum. Infusion with cholecystokinin octapeptide emptied the gall bladder more effectively and predictably and a median of 80 per cent (range 62 to 93 per cent) of the bile had been emptied into the duodenum after one hour. It was concluded that the induction of bile storage in the gall bladder with methadone and the subsequent stimulation of its release into the duodenum by the infusion of cholecystokinin produced an endogenous bile acid load that was three to four times larger than that induced by a meal after a period of fasting.
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